Hypoxia: The force of endometriosis.


Journal

The journal of obstetrics and gynaecology research
ISSN: 1447-0756
Titre abrégé: J Obstet Gynaecol Res
Pays: Australia
ID NLM: 9612761

Informations de publication

Date de publication:
Mar 2019
Historique:
received: 04 12 2018
accepted: 14 12 2018
pubmed: 9 1 2019
medline: 21 6 2019
entrez: 9 1 2019
Statut: ppublish

Résumé

Summarize recent findings of how hypoxia regulates numerous important processes to facilitate the implantation, proliferation and progression of ectopic endometriotic lesions. Most up-to-date evidences about how hypoxia contributes to the disease pathogenesis of endometriosis and potential therapeutic approaches were collected by conducting a comprehensive search of medical literature electronic databases. Quality of data was analyzed by experienced experts including gynecologist and basic scientists. Uterus is a highly vascularized organ, which makes endometrial cells constantly expose to high concentration of oxygen. When endometrial tissues shed off from the eutopic uterus and retrograde to the peritoneal cavity, they face severe hypoxic stress. Even with successful implantation to ovaries or peritoneum, the hypoxic stress remains as a critical issue because endometrial cells are used to live in the well-oxygenated environment. Under the hypoxia condition, cells undergo epigenetic modulation and evolve several survival processes including steroidogenesis, angiogenesis, inflammation and metabolic switch. The complex gene regulatory network driven by hypoxia ensures endometriotic cells can survive under the hostile peritoneal microenvironment. Hypoxia plays critical roles in promoting pathological processes to facilitate the development of endometriosis. Targeting hypoxia-mediated gene network represents an alternative approach for the treatment of endometriosis.

Identifiants

pubmed: 30618168
doi: 10.1111/jog.13900
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

532-541

Subventions

Organisme : Ministry of Science and Technology, Taiwan
ID : MOST 106-2320-B-006-072-MY3

Informations de copyright

© 2019 Japan Society of Obstetrics and Gynecology.

Auteurs

Meng-Hsing Wu (MH)

Department of Obstetrics and Gynecology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

Kuei-Yang Hsiao (KY)

Institute of Biochemistry, National Chung Hsing University, Taichung, Taiwan.

Shaw-Jenq Tsai (SJ)

Department of Physiology, College of Medicine, National Cheng Kung University, Tainan, Taiwan.

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Classifications MeSH